MK-383 (L-700,462) 是一种选择性的非类血小板糖蛋白IIb/IIIa抗剂,在人体中是活跃的
K Peerlinck1, I De Lepeleire, M Goldberg
1Center for Molecular and Vascular Biology, University of Leuven, Belgium.
Circulation
|October 1, 1993
概括
MK-383是一种新的非类糖蛋白IIb/IIIa对抗剂,有效抑制血小板聚合并延长人类的出血时间. 这种药物对开发新的抗血栓治疗有前途.
科学领域:
- 药理学 药理学 是一个学科.
- 心血管医学 心血管医学
- 血液学 血液学 血液学
背景情况:
- 血小板聚合对于血栓形成至关重要,由糖蛋白 (GP) IIb/IIIa的纤维素因子交叉链接介导.
- 抑制这个最后的共同途径提供了一个潜在的抗血栓策略.
- MK-383是一种新型的非型GP IIb/IIIa抗剂.
研究的目的:
- 评估MK-383在人体中的体外和体内活性和耐受性.
- 评估MK-383对血小板聚合和出血时间的影响.
主要方法:
- 在体外研究中评估了MK-383抑制纤维素原与激活血小板的结合.
- 一项对健康男性进行的双盲,安慰剂控制,剂量升级研究评估了静脉注射MK-383输液 (1小时和4小时).
- 测量了ex vivo血小板聚合 (ADP和原诱导) 和模板出血时间.
主要成果:
- 在体外和体外,MK-383证明了对血小板聚合的剂量依赖抑制.
- 在较高剂量时观察到完全的ex vivo血小板聚合抑制.
- 根据剂量,MK-383显著延长了模板出血时间,并使输液后的效果正常化.
结论:
- MK-383在人类中耐受性良好,活跃.
- 它代表了第一个非基GP IIb/IIIa对抗剂,用于研究抗血栓潜力.
- 这种类型的抗血小板药物对抗血小板药物治疗具有前景.
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